In 1985, the authors studied the epidemiology of hepatitis B virus (HBV) in a healthy Middle Eastern population. Residents of three remote villages and urban areas of Jordan were assessed for seroprevalence of hepatitis B surface antigen (HBsAg) and HBV infection. Infection was defined as the presence of antibody to hepatitis B core antigen (total) and/or antibody to hepatitis B surface antigen, with or without HBsAg. The overall HBsAg prevalence was 9.9% and was not age-related, although significant differences were noted between the villages (range, 5.7%-12.8%). The prevalence of HBV infection was 36% and increased with age. In addition, there were differences between the villages in patterns of age-specific infection. A newly constructed socioeconomic index showed greater HBsAg prevalence in lower (14.4%) than in upper (2.4%) socioeconomic groups. A history of contact with a jaundiced person and socioeconomic status were independent risk factors for HBsAg-positive status, while contact with a jaundiced person, rural background, and age were independently related to HBV infection. There was evidence of familial clustering of HBV in two of the villages, with HBV carriers and infected children particularly aggregating around HBsAg-positive siblings. There was also a trend toward an association of HBsAg-positive children with HbsAg-positive mothers. HBV carrier prevalence correlated with family size, and HBV infection in the household increased proportionately with the number of carriers in the family. Hepatitis B e antigen was detected most frequently in children and antibody to hepatitis B e antigen in adults. Postnatal early childhood transmission through contact among children of poorer and larger families probably accounts for the high endemicity of HBV in this region.

The epidemiology and clinical outcome of hepatitis D viral infection in HBsAg-positive acute hepatitis, chronic liver disease, primary hepatocellular carcinoma and the symptomless carrier state was studied in Jordan. The prevalence of hepatitis D viral infection was significantly higher in patients with chronic liver disease (18/79, 23%) and acute hepatitis (17/108, 16%) than in symptomless HBsAg carriers (2/136, 2%). The highest prevalence of hepatitis D viral infection was found in patients with primary hepatocellular carcinoma (10/15, 67%) who were also significantly older than such patients without hepatitis D viral infection. Antihepatitis D virus IgM was detected persistently in 83% of patients with antihepatitis D virus-positive chronic liver disease and transiently in 41% of patients with acute hepatitis. A trend to increased mortality was observed in acute hepatitis D viral superinfection (25%) compared to hepatitis D viral coinfection (0%) and to antihepatitis D virus-negative HBsAg-positive acute hepatitis (4%). In patients with established chronic liver disease, however, neither survival nor histological parameters of disease activity were significantly different in the antihepatitis D virus-positive and antihepatitis D virus-negative groups. While the early stage of hepatitis D viral superinfection is associated with increased mortality, it appears that in patients with late-stage chronic liver disease, severe histological activity subsides, and survival is no longer influenced by the factor of hepatitis D viral infection. However, primary hepatocellular carcinoma appears to complicate the course of those antihepatitis D virus-positive patients surviving beyond this stage.

585ducing strain in Europe indicate the increasing spread of ROB-1 beta-lactamase producing strains among clinical isolates of Haemophilus hzfluenzae. We found that ROB-1 production in strain 86 242 is mediated by a plasmid, designated pCFF 242. Its molecular weight (4,4 Kb) is identical to that of R-ROB from original ROB-1 beta-lactamase producing Haemophilus influenzae. Moreover, digestion patterns with restriction endonucteases of plasmid DNA from strain 86 242 were identical to those of R-ROB. This finding is surprising in view of the geographical origin of the two strains. Medeiros et al. (1) nevertheless reported that plasmids encoding for ROB-t in humanHaernophilus influenzae strains isolated in the USA were strikingly similar, regardless of where they were isolated. However, the close relationship between the ROB-I encoding plasmids of the reference strain and the first strain isolated in Europe is a very interesting observation regarding of the epidemiology of ROB-I producing Haemophihts infIuenzae strains.